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Biomedical subjects

T Takemoto

Publications and source records attributed to T Takemoto.

427 records · Page 24Linked to original sources
PubMedDate not supplied

Clinical evaluation of teprenone, a mucosal protective agent, in the treatment of patients with gastric ulcers: a nationwide, multicenter clinical study.

The recurrence rate of gastric ulcers healing to a white scar is low, whereas that of ulcers healing to a red scar is high. Teprenone is a mucosal protective agent that can promote epithelial regeneration by increasing the mucosal hexosamine content. It promotes white scar formation when administered as maintenance therapy for ulcers. A nationwide, multicenter study was performed to determine whether white scar formation was also promoted when teprenone was used during initial therapy. Analysis of the data from 1249 patients showed that teprenone significantly promoted white scar formation. The presence of severe ulcers (large size and active stage), ulcer location at the gastric angulus, and smoking retarded white scar formation irrespective of the use of teprenone.

Adult↗
PubMedDate not supplied

In vivo cell kinetics studies of the duodenum during and after healing of cysteamine-induced duodenal ulcer in rats using bromodeoxyuridine incorporation.

The present study investigated the defect of duodenal defence responsible for the tendency of recurrence of duodenal ulcer. Male Wistar rats were treated with cysteamine-HCl subcutaneously to induce duodenal ulcer, and bromodeoxyuridine (BrdU) was given intraperitoneally 1 h before laparotomy. Serial tissue sections and immunocytochemical staining of BrdU were done to study the cell kinetics during and after healing. Deep ulcers developed in the proximal part of the duodenum 24 h after cysteamine injection, and the ulcer was replaced by scar tissue 1 week later. BrdU-labelling index of normal duodenal mucosa in control rats was 30-34%. On the peripheral part of the regenerative mucosa, BrdU-labelling index increased from 1.5% to 26-27%, 1-4 weeks after injection and remained at this level thereafter. On the central part, except the most central area, the labelling index remained at 0% until 3 weeks, and was 15% 6 weeks after cysteamine treatment. It never achieved the level seen in control normal mucosa. The labelling rate of fibrous cells in scar tissue decreased from 28% to nearly 0% 1-4 weeks after the injection. It is concluded that both the ulcer scar and the regenerative mucosa do not achieve a mature state in the initial scarred stage; they need more time to reach a relatively mature condition. Moreover, the regenerative mucosa will be the weak, easily damaged part of the duodenum.

Animals↗
PubMedDate not supplied

Role of superoxide dismutase in mechanism of diethyldithiocarbamate-induced gastric antral ulcer in rats: protective effect of prostaglandin, cimetidine and pirenzepine.

The role of superoxide radicals and the protective effects of superoxide dismutase (SOD), allopurinol, 16,16-dimethyl-prostaglandin E2 (dmPGE2), cimetidine and pirenzepine in diethyldithiocarbamate (DDC)-treated rats were evaluated. Pretreatment with Cu,Zn-SOD (superoxide radical scavenger) 60,000 units/kg, allopurinol (competitive inhibitor of xanthine oxidase) 50 mg/kg, dmPGE2 (prostaglandin analogue) 10 micrograms/kg, cimetidine (H2-receptor antagonist) 10 mg/kg or pirenzepine (selective antimuscarinic drug) 10 mg/kg all significantly reduced the DDC-induced (800 mg/kg) gastric antral ulcer formation in rats. DDC treatment substantially decreases the gastric mucosal Cu,Zn-SOD activity. In this study treatment with DDC and SOD, DDC and dmPGE2, DDC and cimetidine, and DDC and pirenzepine were demonstrated significantly to prevent the decrease of gastric mucosal Cu,Zn-SOD activity. However, allopurinol did not have this effect. The results suggest that SOD and/or superoxide radicals may play an important role in the mechanism of DDC-induced gastric antral ulcer. The protective property against ulcer formation of these drugs studied might be due to the action of SOD in the gastric mucosa.

16,16-Dimethylprostaglandin E2↗